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Overt and Latent Cardiac Effects of Ozone Inhalation in Rats: Evidence for Autonomic Modulation and Increased Myocardial Vulnerability
Citation:
FARRAJ, A., M. S. HAZARI, D. W. WINSETT, A. Kulukulalani, A. Carll, N. HAYKAL-COATES, E. LAPPI, C. Lamb, D. TERRELL, W. CASCIO, AND D. L. Costa. Overt and Latent Cardiac Effects of Ozone Inhalation in Rats: Evidence for Autonomic Modulation and Increased Myocardial Vulnerability. ENVIRONMENTAL HEALTH PERSPECTIVES. National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC, 120(3):348-54, (2012).
Impact/Purpose:
We demonstrate that ozone exposure causes several adverse cardiac effects that may be mediated by autonomic dysfunction This is the first study to show that exposure to low ozone concentrations may cause subclinical effects that are only manifested when triggered by a stressor, suggesting that health effects of ambient levels of air pollutants rnay be insidious and poentially underestimated.
Description:
Background: Ozone (03) is a well-documented respiratory oxidant, but increasing epidemiologic evidence points to extra-pulmonary effects including positive associations between ambient 03 concentrations and cardiovascular morbidity/mortality. Objectives: With preliminary reports linking 03 exposure with changes in heart rate (HR), we hypothesized that a single inhalation exposure to 0 3 will cause concentration-dependent autonomic modulation of cardiac function in rats. Methods: Rats implanted with telemeters to monitor HR and the electrocardiogram were exposed once by whole-body inhalation for 4 hr to 0.8 or 0.2 parts per million (ppm) 03 or filtered air. A separate cohort was tested for vulnerability to aconitineinduced arrhythmia 24 hr after exposure. Results: Exposure to 0.8 ppm 03 caused bradycardia, PR prolongation, ST depression, and substantial increases in atrial premature beats (APB), sinoatrial block (SAB) and atrioventricular block (AVB) accompanied by concurrent increases in several heart rate variability (HRV) parameters that were suggestive of increased parasympathetic tone. Low 03 exposure failed to elicit any overt changes in autonomic tone, heart rhythm or the electrocardiogram. However, both 0.2 and 0.8 ppm 0 3 increased sensitivity to aconitine-induced arrhythmia formation, suggesting a latent O3-induced alteration in myocardial excitability. Conclusions: 03 exposure causes several effects on cardiac electrophysiology that are likely mediated by modulation of autonomic input to the heart. Moreover, exposure to low 03 concentrations may cause subclinical effects that are only manifested when triggered by a stressor, suggesting that health effects of ambient levels of air pollutants may be insidious and potentially underestimated (This abstract does not reflect EPA policy).
